Galectin-3 is upregulated in microglial cells in response to ischemic brain lesions, but not to facial nerve axotomy

We have recently demonstrated that the beta-galactoside-specific lectin gal ectin-3 is expressed by microglial cells in vitro, but not by normal restin g microglia in vivo. In the present study, we have analyzed the expression of galectin-3 by microglia under traumatic conditions in vivo using two exp erimental rat models which substantially differ in the severity of lesion r elated to a breakdown of the blood-brain barrier (BBB) and the occurrence o f inflammatory processes. These two features are absent after peripheral ne rve lesion and present after cerebral ischemia. Here we show that, followin g facial nerve axotomy under conditions allowing (nerve anastomosis) or not subsequent regeneration (nerve resection), galectin-3 is not expressed by microglia in the corresponding facial nucleus 1-112 days after lesion. Gale ctin-3 is also absent in microglia at sites of a defective BBB in the norma l brain, such as the circumventricular organs. Following experimental ische mia (i.e., permanent occlusion of the middle cerebral artery), in contrast, galectin-3 becomes strongly expressed by activated microglia as early as 4 8 hours after trauma, as determined by immunohistochemistry and Western blo t analysis. Our findings suggest that the expression of galectin-3 by micro glia in vivo correlates with the state of microglial activation. (C) 2000 W iley-Liss, Inc.